Rebalancing the commissural system: mechanisms of vestibular compensation

Abstract

Vestibular compensation after unilateral vestibular loss is a complex, multi-factored process involving synaptic and neuronal plasticity in many areas of the brain, and it is a challenge to identify the key sites of plasticity that determine the rate and extent of behavioural recovery. Experimental evidence strongly implicates the vestibular commissural inhibitory system which links the brainstem vestibular nuclei of the two sides, both in causing the initial severe oculomotor and postural symptoms of vestibular deafferentation, and in the subsequent recovery that takes place in the early stages of compensation. Of particular interest are changes in GABAergic neurotransmission within the commissural system, and the possibility that histaminergic drugs as well as stress steroids and neurosteroids that can modulate compensation, may do so at least in part by their effects on commissural inhibition. A fuller understanding of the role of the commissural system in compensation and the effects of GABAergic neuromodulators is likely to reveal the mechanisms of action of histamine in the vestibular system and the interactions between stress, anxiety and vestibular dysfunction.